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Park, Chun,Kim, Jung Ran,Shin, Jae Kyoung,Kim, June Ki,Lee, Tae Kyun,Chung, Ji Chun,Park, Weon Hwan,Park, Sun Dong,Nam, Kyung Soo,Lee, Young Choon,Kim, Cheorl Ho 한국키틴키토산학회 1997 한국키틴키토산학회지 Vol.2 No.2
A mycelial chitin deacetylase has been purified from a chitin deacetylase-hyperproducing fungus, Absidiα coerulea CHK-1. The purified enzyme had a molecular mass of about 62 kDa on denaturated and natural conditions. The pI was 5.5. The chitin deacetylase, when resolved by SDS-PAGE, was positive for Schiff staining, suggesting that the enzyme is a glycoprotein. When O-hydroxylated chitin (glycolchitin) was used as a substrate, the enzyme displayed a temperature optimum of around 50℃ and a pH optimum of around PH 5,5. The enzyme was stable to incubation from pH 3.0 to pH 6.5 at 4℃ for 24 hr. The presence of chitin protected the enzyme from heat inactivation, the extent depending upon the substrate concentration. The activity of the enzyme was stimulated by Mn2+ ion. The enzyme is active on chitooligosaccharides with more than two N-acetylglucosamine residues (M-acetylchitobiose). However, the enzyme is not active on N-acetylglucosamine. The enzyme had an apparent Km of 12.4 mM and Kcat of 32.4 /sec for glycol chitin, respectively.
Shin, Seungwon,Kim, Jinyoung,Yu, Ami,Seo, Hyung-Sik,Shin, Mi-Ran,Cho, Jae-Heung,Yi, Gilhee,Hong, Seung-Ug,Lee, Euiju Hindawi 2017 Evidence-based Complementary and Alternative Medic Vol.2017 No.-
<P>This study protocol aims to explore the effectiveness, safety, and cost-effectiveness of a herbal medication,<I> Gongjindan</I> (GJD), in patients with chronic dizziness. This will be a prospective, multicenter, randomized, double-blind, placebo-controlled, parallel-group, clinical trial. Seventy-eight patients diagnosed with Meniere's disease, psychogenic dizziness, or dizziness of unknown cause will be randomized and allocated to either a GJD or a placebo group in a 1 : 1 ratio. Participants will be orally given 3.75 g GJD or placebo in pill form once a day for 56 days. The primary outcome measure will be the Dizziness Handicap Inventory score. Secondary outcome measures will be as follows: severity (mean vertigo scale and visual analogue scale) and frequency of dizziness, balance function (Berg Balance Scale), fatigue (Fatigue Severity Scale) and deficiency pattern/syndrome (qi blood yin yang-deficiency questionnaire) levels, and depression (Korean version of Beck's Depression Inventory) and anxiety (State-Trait Anxiety Inventory) levels. To assess safety, adverse events, including laboratory test results, will be monitored. Further, the incremental cost-effectiveness ratio will be calculated based on quality-adjusted life years (from the EuroQoL five dimensions' questionnaire) and medical expenses. Data will be statistically analyzed at a significance level of 0.05 (two-sided). This trial is registered with ClinicalTrials.gov NCT03219515, in July 2017.</P>
Complete Nucleotide Sequence of Cytochrome P450 2E1 Expressed in the Rat Brain
Shin, Song-Woo,You, Kwan-Hee,Ryu, Hye-Myung,Kim, Su-Won,Kwon, Oh-Sik,Song, Jae-Chan,Kim, Myoung-Hee,Kim, Dae-Ran,Yoo, Min 대한의생명과학회 2005 Biomedical Science Letters Vol.11 No.2
2-Deoxyribonolactone (dL) arises as a major DNA damage induced by a variety of agents, involving free radical attack and oxidation of C1'-deoxyribose in DNA. We investigated whether dL lesions can be repaired in mammalian cells and the mechanisms underlying the role of DNA polymerase β in processing of dL lesions. Pol β appeared to be trapped by dL residues, resulting in stable DNA-protein cross-links. However, repair DNA synthesis at site-specific dL sites occurred effectively in cell-free extracts, but predominantly accompanied by long-patch base excision repair (BER) pathway. Reconstitution of long-patch BER demonstrated that FEN 1 was capable of removing the displaced flap DNA containing a 5'-dL residue. Cellular repair of dL lesions was largely dependent on the DNA polymerase activity of Pol β. Our observations reveal repair mechanisms of dL and define how mammalian cells prevent cytotoxic effects of oxidative DNA lesions that may threaten the genetic integrity of DNA.From the RT-PCR amplifications using mRNA templates isolated from Sprague-Dawley rat brains, we isolated a cDNA fragment of 1,524 bp which covered the full coding information of the rat brain CYP2E1. Its nucleotide sequence was identical to the previously reported rat liver CYP2E1 mRNA except for the difference of one base (A to C at the nucleotide position 73). This difference also altered the amino acid Lys to Gln. However, no insertion or deletion of nucleotide(s) which could alter the reading frame was found within the structure of this rat brain CYP2E1. This study should provide the molecular basis regarding the pathophysiological function of CYP2E1 in the brain.